Evidence map›Paper›PMID 38161333›Full record

ReviewFrontiers in cell and developmental biology2023

ATP-induced cell death: a novel hypothesis for osteoporosis.

Wei Wang, Haolong Zhang, Doblin Sandai, Rui Zhao, Jinxia Bai, Yanfei Wang, Yong Wang, Zhongwen Zhang, Hao-Ling Zhang, Zhi-Jing Song

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 14 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Wei WangCollege of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Haolong ZhangDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Penang, Malaysia.
Doblin SandaiDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Penang, Malaysia.
Rui ZhaoClinical College of Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Jinxia BaiCollege of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Yanfei WangCollege of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Yong WangPathology Center, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Zhongwen ZhangSchool of Public Health, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Hao-Ling ZhangDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Penang, Malaysia.
Zhi-Jing SongClinical College of Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Gansu University of Traditional Chinese Medicine · CNUniversiti Sains Malaysia · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATP-induced cell death has emerged as a captivating realm of inquiry with profound ramifications in the context of osteoporosis. This study unveils a paradigm-shifting hypothesis that illuminates the prospective involvement of ATP-induced cellular demise in the etiology of osteoporosis. Initially, we explicate the morphological attributes of ATP-induced cell death and delve into the intricacies of the molecular machinery and regulatory networks governing ATP homeostasis and ATP-induced cell death. Subsequently, our focus pivots towards the multifaceted interplay between ATP-induced cellular demise and pivotal cellular protagonists, such as bone marrow-derived mesenchymal stem cells, osteoblasts, and osteoclasts, accentuating their potential contributions to secondary osteoporosis phenotypes, encompassing diabetic osteoporosis, glucocorticoid-induced osteoporosis, and postmenopausal osteoporosis. Furthermore, we probe the captivating interplay between ATP-induced cellular demise and alternative modalities of cellular demise, encompassing apoptosis, autophagy, and necroptosis. Through an all-encompassing inquiry into the intricate nexus connecting ATP-induced cellular demise and osteoporosis, our primary goal is to deepen our comprehension of the underlying mechanisms propelling this malady and establish a theoretical bedrock to underpin the development of pioneering therapeutic strategies.

Indexed as

apoptosisATP-induced cell deathautophagybone marrow-derived mesenchymal stem cellscomplicationsosteoblastsosteoclastsosteoporosis

Identifiers

PMID38161333
PMCPMC10755924
OpenAlexW4389734439

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.